TRPV3 expression and vasodilator function in isolated uterine radial arteries from non-pregnant and pregnant rats

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• 作者：Timothy V. Murphy^a ; ^{tim.murphy@unsw.edu.au" class="auth_mail" title="E-mail the corresponding author} ; Arjna Kanagarajah^a ; Sianne Toemoe^a ; Paul P. Bertrand^a ; T. Hilton Grayson^a ; Fiona C. Britton^a ; Leo Leader^b ; Sevvandi Senadheera^a ; Shaun L. Sandow^a ; ^c
• 关键词：TRPV3 ; Carvacrol ; Uterus ; Radial artery ; Pregnancy
• 刊名：Vascular Pharmacology
• 出版年：2016
• 出版时间：August 2016
• 年：2016
• 卷：83
• 期：Complete
• 页码：66-77
• 全文大小：1946 K

文摘

This study investigated the expression and function of transient receptor potential vanilloid type-3 ion channels (TRPV3) in uterine radial arteries isolated from non-pregnant and twenty-day pregnant rats. Immunohistochemistry (IHC) suggested TRPV3 is primarily localized to the smooth muscle in arteries from both non-pregnant and pregnant rats. IHC using C′ targeted antibody, and qPCR of TRPV3 mRNA, suggested pregnancy increased arterial TRPV3 expression. The TRPV3 activator carvacrol caused endothelium-independent dilation of phenylephrine-constricted radial arteries, with no difference between vessels from non-pregnant and pregnant animals. Carvacrol-induced dilation was reduced by the TRPV3-blockers isopentenyl pyrophosphate and ruthenium red, but not by the TRPA1 or TRPV4 inhibitors HC-030031 or HC-067047, respectively. In radial arteries from non-pregnant rats only, inhibition of NOS and sGC, or PKG, enhanced carvacrol-mediated vasodilation. Carvacrol-induced dilation of arteries from both non-pregnant and pregnant rats was prevented by the IK_Ca blocker TRAM-34. TRPV3 caused an endothelium-independent, IK_Ca-mediated dilation of the uterine radial artery. NO-PKG-mediated modulation of TRPV3 activity is lost in pregnancy, but this did not alter the response to carvacrol.